Hyperbaric medicine

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Hyperbaric medicine, also known as hyperbaric oxygen therapy (HBOT) is the medical use of oxygen at a higher than atmospheric pressure.


Several therapeutic principles are made use of in HBOT:

  • The increased overall pressure is of therapeutic value when HBOT is used in the treatment of decompression sickness and air embolism.
  • For many other conditions, the therapeutic principle of HBOT lies in a drastically increased partial pressure of oxygen in the tissues of the body. The oxygen partial pressures achievable under HBOT are much higher than those under breathing pure oxygen at normobaric conditions (i.e. at normal atmospheric pressure).
  • A related effect is the increased oxygen transport capacity of the blood. Under atmospheric pressure, oxygen transport is limited by the oxygen binding capacity of hemoglobin in red blood cells and very little oxygen is transported by blood plasma. Because the hemoglobin of the red blood cells is almost saturated with oxygen under atmospheric pressure, this route of transport can not be exploited any further. Oxygen transport by plasma, however is significantly increased under HBOT.

The United States, the Undersea and Hyperbaric Medicine Society -- "UHMS" approved for reimbursement diagnoses for application of HBOT in hospitals such as:

In the United States, HBOT is recognized by Medicare as a reimbursable treatment for 14 UHMS "approved" conditions. An HBOT session costs anywhere from $100 to $200 in private clinics, to over $1,000 in hospitals. More U.S. physicians are lawfully prescribing HBOT for "off label" conditions such as Lyme Disease and stroke. Such patients are treated in outpatient clinics, however it is unlikely that their medical insurance will pay for off label treatments. In the United Kingdom most chambers are financed by the National Health Service, although some, such as those run by Multiple Sclerosis Therapy Centres, are non-profit.

HBOT is controversial and health policy regarding its uses is politically charged. Both sides of the controversy on the effectiveness of HBOT is available in the form of PUBMED and the Cochrane reviews[1] and a discussion of "Medical Polemics"[2], a discussion of Multiple Sclerosis in particular [3].

The chamber


The traditional type of hyperbaric chamber used for HBOT is a hard shelled pressure vessel. Such chambers can be run at absolute pressures up to 600 kilopascals or 85 PSI (lbf/in²), nearly six atmospheres.

Navies, diving organizations and hospitals typically operate these. They range in size from those which are portable and capable of transporting just one patient to those which are fixed, very heavy and capable of treating eight or more patients.

The chamber may consist of:

  • a pressure vessel that is generally made of steel and aluminium with the view ports (windows) or hull made of acrylic.
  • one or more human entry hatches—these could be small and circular or wheel-in type hatches for patients on trolleys
  • an airlock allowing human entry—a separate chamber with two hatches, one to the outside world and one to the main chamber, which can be independently pressurized to allow patients to enter or exit the main chamber while it is still pressurized
  • an airlock allowing medicines, instruments and food to enter the main chamber
  • glass ports or closed-circuit television allowing the technicians and medical staff outside the chamber to monitor the inside of the chamber
  • an intercom allowing two-way communications inside and outside the chamber
  • a carbon dioxide scrubber—consisting of a fan that passes the gas inside the chamber through a soda lime canister
  • a control panel outside the chamber is used to open and close valves allowing air to enter or leave the chamber and oxygen to be supplied to masks

Oxygen Breathing

Breathing 100% oxygen from a aviators oxygen mask.

In larger "multiplace" chambers, both patients and medical staff inside the chamber may breathe from tightly fitting aviators type oxygen masks, which supply pure oxygen and remove the exhaled gas from the chamber. Or they may breathe from "oxygen helmets", flexible, transparent soft plastic helmets with a seal around the neck somewhat similar to a space suit helmet. During treatment patients breathe 100% oxygen most of the time but have periodic air breaks to minimize the risk of oxygen toxicity. The exhaled gas must be removed from the chamber to prevent the build up of oxygen, which could provoke a fire. Medical staff may also breathe oxygen to reduce the risk of decompression sickness. Administration of 100% breathing oxygen maximizes the patients treatment. The pressure inside the chamber is increased by opening valves allowing high-pressure air to enter from storage cylinders, similar to diving cylinders. A gas compressor is used to fill these cylinders.

A recompression chamber for a single diving casualty

Smaller "monoplace" chambers can only accommodate the patient. No medical staff can enter. The chamber is flooded with pure oxygen or compressed air. The cost of using pure oxygen in a monoplace chamber is much higher then using compressed air. If pure oxygen is used no oxygen breathing mask or helmet is needed. If compressed air is used then a oxygen mask or helmet is needed as in a multiplace chamber. In monoplace chambers that are compressed with pure oxygen a mask is available to provide the patient with "air breaks," periods of breathing normal air, in order to reduce the risk of hyperoxic seizures.

Effects of Pressure

Patients inside the chamber will notice discomfort inside their ears as a pressure difference develops between their middle ear and the chamber atmosphere. This can be relieved by the Valsalva maneuver or by "jaw wiggling". As the pressure increases further, mist may form in the air inside the chamber and the air may become warm. When the patient speaks, the pitch of the voice may increase to the level that they sound like cartoon characters.

To reduce the pressure, a valve is opened to allow gas out of the chamber. As the pressure falls, the patient’s ears may "squeak" as the pressure inside the ear equalizes with the chamber. The temperature in the chamber will fall.

Home treatment

There are portable HBOT chambers, which are used for home treatment. These are usually referred to as "mild chambers", which is a reference to the lower pressure of soft-sided chambers. Those commercially available in the USA go up to 4.1 PSI (about 28.268 kPa) overpressure which is equivalent to a water depth of 11 ft. These chambers are operated with oxygen concentrators or with 100% oxygen as the breathing gas. The soft chambers are FDA approved only for the treatment of Altitude Sickness. In addition, the FDA has a specific warning that supplemental oxygen is not to be used.


Historical link to diving

Initially, HBOT was developed as a treatment for diving disorders involving bubbles of gas in the tissues, such as decompression sickness and gas embolism. The chamber cures decompression sickness and gas embolism by increasing pressure, reducing the size of the gas bubbles and improving the transport of blood to downstream tissues. The high concentrations of oxygen in the tissues are beneficial in keeping oxygen-starved tissues alive, and have the effect of removing the nitrogen from the bubble, making it smaller until it consists only of oxygen which is then re-absorbed into the body. After elimination of bubbles, the pressure is gradually reduced back to atmospheric levels.


The slang term for a cycle of pressurization inside the HBOT chamber is "a dive". An HBOT treatment for longer-term conditions is often a series of 20 to 40 dives.

Emergency HBOT for diving disorders typically follows one of two forms. For most cases, a shallow "dive" to a pressure the equivalent of 18 meters / 60 feet of water for 3 to 4.5 hours with the casualty breathing pure oxygen with air breaks every 20 minutes to reduce oxygen toxicity. For extremely serious cases, a deeper "dive" to a pressure the equivalent of 37 meters / 122 feet of water for 4.5 hours with the casualty breathing air.

In Canada and the United States, the U.S. Navy Dive Charts are used to determine the duration, pressure and breathing gas of the therapy. The most frequently used tables are Table 5 and Table 6. In the UK the Royal Navy 62 and 67 tables are used.

The Undersea and Hyperbaric Medical Society[4] (UHMS) publishes a report which compiles the latest research findings and contains information regarding the recommended duration and pressure of the longer-term conditions.

Possible complications

There are risks associated with HBOT, similar to some diving disorders. Pressure changes can cause a "squeeze" or barotrauma in the tissues surrounding trapped air inside the body, such as the lungs, behind the eardrum, inside paranasal sinuses, or trapped underneath dental fillings. Breathing high-pressure oxygen for long periods can cause oxygen toxicity. Temporarily blurred vision can be caused by swelling of the lens, which usually resolves in two to four weeks.

The only absolute contraindication to hyperbaric oxygen therapy is untreated pneumothorax. Relative complications include grand mal seizure, fever, the inability to clear the ears or sinuses, and the use of certain chemotherapy agents.

There are reports that cataract may progress following HBOT. Also a rare side effect has been blindness secondary to optic neuritis (inflammation of the optic nerve).


study on HBOT used for wound healing found that cigarette smoking was associated with poor response (p<0.0001), while diabetes was not. The same study found that high levels of blood creatinine, urea nitrogen, and young age improved response to HBOT.


The Collet (Quebec) trial[5] that was published in the Lancet in 2001 was the largest randomized trial of Hyperbaric Oxygen Therapy (HBOT) for children with cerebral palsy (CP); it followed the McGill pilot study on the same subject[6].

The evidence showed that both groups of children treated with two very different hyperbaric treatment dosages improved significantly. The motor improvements that were seen and measured with the gross motor function measure[7] were greater, more generalized, and were obtained in a shorter period of time than most of the changes found in any other studies of recognized conventional therapies in the treatment of children with cerebral palsy[8] [9]. The children in both groups improved an average of ten times more during the two months of HBOT (whilst all other therapies and medication were stopped) than during the three months follow-up (when medication and all the ancillary treatments were restarted). This impressive change in the rate of improvements clearly indicates the probable effectiveness of hyperbaric treatment. Both the Lancet commentary[10] and the tech report by the Agency for Healthcare Research and Quality (AHRQ)[11] concluded that the hypothesis of both treatments being equally effective should be retained, possibly as the main hypothesis.

Since the Quebec study of HBOT for children with CP, many reports[12] [13] have been made on the possible efficacy of a low pressure hyperbaric treatment and all the trials [14] [15] [16] [17] conducted with HBOT in CP have demonstrated positive results.

Middle ear barotrauma (MEBT) is always a consideration in treating both children and adults in a hyperbaric environment, but most children currently being treated with HBOT for autism are being pressurized to 1.3 ATA which greatly reduces the risks of potential side effects of any kind.

Muller-Bolla[18] states that: "This study shows that exposure to low hyperbaric pressure is associated with minor signs of barotrauma compared to very low exposure. All other side effects were rare and similar in both groups."

Several studies in the literature show that markers of hypoxia in the autistic brain are higher than in control brains.[19] [20] [21] [22] This is important because one of the most important mechanisms of HBO protection is the inhibition of apoptosis in hypoxia-ischemia. Inhibition of apoptosis by HBO translates into brain tissue preservation. HBO decreases the activity and expression of capase-3, reduces PARP cleavage, and abolishes DNA fragmentation. HBO causes the up-regulation of pro-survival Bc1-2 genes, protects the blood brain barrier, and improves metabolism of glutamate, glucose, and pyruvate. HBO decreases hypoxia-inducible factor-1a (hip-1a) and multiple genes related to apoptosis. In fact, HBO reduces all pathological events consequent to hypoxia.

Fischer et al.[23] in New York University performed the first randomized, placebo-controlled, double-blind trial on MS patients treated with HBOT. Improvements in balance and bladder function were found in 12 of 17 patients (p<0.0001). Those patients with a less severe form of the disease had a more favorable and long lasting response. After a year with no further treatment, the treated group showed a positive change (p<0.0008). Barnes et al.[24] found overall benefit in their treated group (p<0.03) and a year later there was less deterioration in cerebellar function (p<0.03). Two other controlled studies[25][26] have reported sustained benefit with follow-up.


  1. The Cochrane reviews
  2. Medical Polemics
  3. Discussion of MS
  4. Undersea and Hyperbaric Medical Society
  5. Collet, J.P., Vanasse, M., Marois, P., Amar, M., Goldberg, J., Lambert, J. et al. (2001) Hyperbaric oxygen for children with cerebral palsy: A randomized multicentre trial. The Lancet, 357, 582-586.
  6. Montgomery, D., Goldberg, J., Amar, M., Lacroix, V., Lecomte, J., Lambert, J., Vanasse, M., & Marois, P. (1999). Effects of hyperbaric oxygen therapy on children with spastic diplegic cerebral palsy: A pilot project. Undersea and Hyperbaric Medicine, 26(4), 235-242.
  7. Russell, D.J., Rosenbaum, P.L., Cadman, D.T., Gowland, C., Hardy, S., & Jarvis, S. (1989). The gross motor function measure: A means to evaluate the effects of physical therapy. Developmental Medicine & Child Neurology, 31(3), 341-352.
  8. Almeida, G.L., Campbell, S.K., Girolami, G.L., Penn, R.D., & Corcos, D.M. (1997). Multidimensional assessment of motor function in a child with cerebral palsy following intrathecal administration of baclofen. Physical Therapy, 77 (7), 751-764.
  9. Damiano, D.L. & Abel, M.F. (1998). Functional outcomes of strength training in spastic cerebral palsy. Archives of Physical Medicine and Rehabilitation, 79 (2), 119-125.
  10. Talking Points, Hyperbaric oxygen: Hype or hope? Lancet 2001;357
  11. Agency for Healthcare US Department. (2003). Web page
  12. Chang CF, Niu KC, Hoffer BJ, Wang Y, Borlongan CV. Hyperbaric oxygen therapy for treatment of post ischemic stroke in adult rats. Exp Neurol 2002; 166: 298-306.
  13. Heuser G, Heuser SA, Rodelander D, Aguilera O, Uszler M. Treatment of neurologically impaired adults and children with "mild" hyperbaric oxygenation (1.3 ATA and 24% Oxygen). In Joiner JT, ed. Hyperbaric Oxygenation for Cerebral Palsy and the Brain-Injured Child. Best Publications, Flagstaff Arizona 2002;109-15
  14. Barret, K. (1999). Pediatric cerebral palsy treated by 1.5 ATA hyperbaric oxygen – A pilot study. Proceedings of The Second International Symposium on HBO for CP .
  15. Marois, P., & Vanasse, M. (Juillet 2006). HBOT in the treatment of cerebral palsy: A retrospective study of 120 cases-5 years. Paper presented at 5th Annual Symposium: HBO and the recoverable brain, Fort Lauderdale, USA.
  16. Nighoghossian N., Trouillas P., Adeleine P., Salord F. Hyperbaric oxygen in the treatment of acute ischemic stroke. Stroke 1995; 26: 1369-1372.
  17. SHI Xiao-yan, TANG Zhong-quan, SUN Da and HE Xiao-jun. Evaluation of hyperbaric oxygen treatment of neuropsychiatric disorders following traumatic brain injury. Chin Med J 2006;119(23):1978-1982.
  18. Muller-Bolla M., Collet J.P., Ducruet T., Robinson A. Side effects of hyperbaric oxygen therapy in children with cerebral palsy. Undersea and Hyperbaric Medicine 2006, Vol. 33, No 4
  19. Fatemi, S.H., A.R. Halt, 2001. Altered levels of Bcl2 and p53 proteins in parietal cortex reflect deranged apoptotic regulation in autism. Synapse, 42:281-284
  20. Araghi-Niknam, M., S.H Fatemi, 2003. Levels of Bcl-2 and P53 are altered in superior frontal and cerebellar cortices of autistic subjects. Cell Mol. Neurobiol., 23:945-952.
  21. Fatemi SH, Stary JM, Halt AR, Realmuto GR. Dysregulation of Reelin and Bcl-2 proteins in autistic cerebellum. J Autism Dev Disord. 2001 Dec;31(6):529-35.
  22. Fatemi SH, Halt AR, Stary JM, Realmuto GM, Jalali-Mousavi M. Reduction in anti-apoptotic protein Bcl-2 in autistic cerebellum. Neuroreport. 2001 Apr 17;12(5):929-33.
  23. Fischer BH, Marks M, Reich T. Hyperbaric-oxygen treatment of multiple sclerosis: a randomized, placebo-controlled, double-blind study. N Engl J Med 1983; 308:181-6.
  24. Barnes MP, Bates D, Cartlidge NEF, et al. Hyper-baric oxygen and multiple sclerosis: short term results of a placebo-controlled, double-blind trial. Lancet 1985; ii:297-3006.
  25. Oriani G, Barbieri S, Cislaghi G, Albonico G et al. Hyperbaric oxygen in multiple sclerosis: a placebo-controlled, double-blind, randomized study with evoked potential studies. J Hyp Med 1990; 5: 237-45.
  26. Pallotta R, Anceschi S, Costilgliola N, et al. Prospecttive di terapia iperbarica nella sclerosi a placce. Ann Med Nav 1980; 85: 57-62.

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